The level of cardiovascular event risk is strongly associated with platelet activity. The most important function of platelets is their ability to aggregate, forming clots and preventing extensive bleeding. Aggregation starts by activation of the platelets, which is generally associated with phosphorylation of NADPH oxidase and the production of a signaling compound—superoxide radical. Activation of platelets may be triggered in many different ways. When being measured, platelet aggregation is most commonly triggered by chemical substances. For example, several substances (agonists) such as collagen and ADP are able to bind to receptors on the platelet surface and start the cascade process of activation and aggregation. Antiplatelet activity is often associated with the ability of certain substances (e.g., aspirin) to block these triggering receptors. However, considering the differing and unknown mechanisms of many natural compounds, alternative mechanisms of action may also be operating to reduce or inhibit platelet activation and/or aggregation.